Inhibitory effect of compound W3D on LPS-induced release of inflammatory mediators of RAW264.7 cells through TLR4-MyD88-NF-κB signaling pathway
10.3969/j.issn.1001-1978.2018.07.017
- VernacularTitle:化合物W3D通过调控TLR4-MyD88-NF-κB通路抑制LPS诱导的RAW264.7细胞炎症因子的释放
- Author:
Jie-Ran LUO
1
;
Bei ZHAO
;
Li TANG
;
Rui GE
;
Qing-Shan LI
Author Information
1. 山西医科大学药学院
- Keywords:
benzoxazolone derivative W3D;
RAW264.7 cells;
inflammation;
TLR4;
MyD88;
NF-κB;
inflammatory mediators
- From:
Chinese Pharmacological Bulletin
2018;34(7):977-982
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of the novel benzoxazolone derivative 4-( 5′-dimethylamino )-naph-thalenesulfonyl-2 ( 3H )-benzoxazolone ( W3D ) on TLR4-MyD88-NF-κB signaling pathway in LPS-in-duced RAW264.7 cells. Methods The cell viability was detected by MTT assay, and the contents of TNF-α, IL-6, IL-1β and COX-2 in the cell supernatant were analyzed using ELISA methods. The protein ex-pression of IL-6, TLR4, MyD88, p-IRAK4 and NF-κB were investigated by western blot analysis, and the mRNA expressions of TLR4, MyD88 and IL-6 were an-alyzed by RT-PCR. Results W3D could obviously in-hibit the production of TNF-α, IL-6 and IL-1β in LPS- induced RAW264.7 cell supernatant, but it had no effect on the release of COX-2. Compared with the model group, the expressions of TLR4, MyD88 and IL-6 were decreased significantly in a dose dependent manner. Meanwhile, the expressions of p-IRAK4 and nucleus of NF-κB were decrease in W3D treated group compared with the model group. Conclusion The no-vel compound W3D could inhibit the release of the in-flammatory mediators through the regulation of TLR4-MyD88-NF-κB signaling pathway.
